Stack for Height and Dimo - GTFIH

damn reading through this thread has been hella informative on AAS in general, still definitely considering my options as idrc about my plates getting raped(only looking for appositional growth)
Well if your main goal isnt height then I would go for his stack since its still good for other things like dimo. You can still grow with this stack but isnt really efficient imo
 
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Well if your main goal isnt height then I would go for his stack since its still good for other things like dimo. You can still grow with this stack but isnt really efficient imo
Throwing around these claims like you gave a molecule of evidence on your retarded claims. Reply to me faggot.
 
Iont see em boyo, you did sound like GPT at the start.

Shifting the burden of proof
View attachment 5352069

You yet again failed to provide an actual mechanism and any evidence that Andorgen Receptor agonism leads to fusion while not using the variable e2.


Yet again how does this contradict me?
1st I did send yiu the links, you prob over looked it.

Also I gen want to see this study and im not shiftinf it since I still provided you with sources and explenations
 

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Throwing around these claims like you gave a molecule of evidence on your retarded claims. Reply to me faggot.
I did, chill your ass still writing so be patient and stop whinning
 
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Not really. Im pretty clueless tbh :D. Please document how your topical rosiglitazone is going. Im really intrested in that gang.
yea im going to make a guide but I've been holding off till i saw actual results on myself, in theory it totally works, have some other guides planned
just need money :feelsrope:
 
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Well if your main goal isnt height then I would go for his stack since its still good for other things like dimo. You can still grow with this stack but isnt really efficient imo
i dont need to grow at all lol im well above average in height im just really lacking in secondary characteristics
 
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1st I did send yiu the links, you prob over looked it.

Also I gen want to see this study and im not shiftinf it since I still provided you with sources and explenations
The claim was, you can't lower local e2 without nuking your systemic e2. You are shifting the burden of proof as you should be able to give me a source or hypothesis which is bioligically plausible that you can lower local e2 without nuking systemic. Again, reading comprehension.
6498857 1782488061599


You are denying a well established fact/theory, meaning you are shifting the burden of proof.
Runx2 involved in bone formation
Straight up asked GPT. I don't see the connection between a 5th caspase discovered in fruitflies. This study is completely irrelevant and RunX2 is not mentioned once.
Gp cells responding directly to androgens.
Link 2
The study is claiming that DHT without Estrogen Receptors IN RATS and they concluded suprisingly that Whichever receptor they block out its activity (AR, ERA or ERB) DHT does not form PKC activation. They also did not mention the height of these rats and soley their PKC activation, they concluded ERα, ERβ, and AR cooperate by forming membrane-associated receptor complexes within caveolae. Again, we are not knocking out the receptors, we are nuking oeastradiol and we are not rats, this is all just speculation. Again, this study is not that relevant.

Im really tired so I just skimmed the paper.
 
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Throwing around these claims like you gave a molecule of evidence on your retarded claims. Reply to me faggot.
So correct me if Im wrong about your idea.

So your claim is you can use aas when eliminating e2 and having "0 test" therefor Runx2 wont increase or what?

Tell me abt it
 
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yea im going to make a guide but I've been holding off till i saw actual results on myself, in theory it totally works, have some other guides planned
just need money :feelsrope:
Tag me:02Woop:
 
yea im going to make a guide but I've been holding off till i saw actual results on myself, in theory it totally works, have some other guides planned
just need money :feelsrope:
Tag me, im interested
 
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So correct me if Im wrong about your idea.

So your claim is you can use aas when eliminating e2 and having "0 test" therefor Runx2 wont increase or what?

Tell me abt it
Never said it won't increase, just said its plausible that it won't be net negative due to having an optimal enviroment (nuked e2).
 
Never said it won't increase, just said its plausible that it won't be net negative due to having an optimal enviroment (nuked e2).
so in short you mean to say that your claim is that even if Runx2 or other androgen mediated pathways increase, suppressing E2 shifts the balance enought that the effect will be neutral or even positive on FAH? Is that your claim?
 
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yea bout the only thing i succeeded with genes, i looked into nanadrolone and its said to be one of the lesser 19-nor androgens, tren seems better idrk
 
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yea bout the only thing i succeeded with genes, i looked into nanadrolone and its said to be one of the lesser 19-nor androgens, tren seems better idrk
Idk dude. Pretty clueless, go for tren if you say so. Don’t ask me.
 
so in short you mean to say that your claim is that even if Runx2 or other androgen mediated pathways increase, suppressing E2 shifts the balance enought that the effect will be neutral or even positive on FAH? Is that your claim?
It’s biologically plausible. The main reason RunX2 is thought to lead to fusion is due to local e2 production through Aromatese. Assuming you have no test there is nothing to aromatase. Don’t you think? We don’t have any real evidence other then Aromatese defent men being 6 foot 8. we are basically mimicking their lack of ERA agonism. Instead of getting this genetically we do it with Pharma.
 
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It’s biologically plausible. The main reason RunX2 is thought to lead to fusion is due to local e2 production through Aromatese. Assuming you have no test there is nothing to aromatase. Don’t you think? We don’t have any real evidence other then Aromatese defent men being 6 foot 8. we are basically mimicking their lack of ERA agonism. Instead of getting this genetically we do it with Pharma.
I agree with the last part. Didnt say theoreticlly impossible. Issue is how do you know that its gonna weigh it out from the maturation. Lets agree that whenever you take something like hgh or aas it will mature your bones, this just makes sense because you are growing the bones and this will literally mature it. And even if Im wrong, lets say somehow the maturation doesnt exist when using Dht derivatives. How will you achieve no test long term, enough to see some growth?
 
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I agree with the last part. Didnt say theoreticlly impossible. Issue is how do you know that its gonna weigh it out from the maturation. Lets agree that whenever you take something like hgh or aas it will mature your bones, this just makes sense because you are growing the bones and this will literally mature it. And even if Im wrong, lets say somehow the maturation doesnt exist when using Dht derivatives. How will you achieve no test long term, enough to see some growth?
How would it mature your bones? I have never seen an example where anything ever matured your bones without the e2 variable. :feelswhy:
 
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How would it mature your bones? I have never seen an example where anything ever matured your bones without the e2 variable. :feelswhy:
This one states abt hgh
and this abt anavar for example
This study shows that low dose anavar DOES increase height velocity BUT weighs it out by speeding up the maturation
So at the end no real FAH increase.

I even marked it for you so you dont say that it doesnt state shit

Now I awnsered your question and you awnser mine from the last reply.
 

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This one states abt hgh
and this abt anavar for example
This study shows that low dose anavar DOES increase height velocity BUT weighs it out by speeding up the maturation
So at the end no real FAH increase.

I even marked it for you so you dont say that it doesnt state shit

Now I awnsered your question and you awnser mine from the last reply.
Dude I’m not even gonna keep arguing with your retarded studies. In neither of those studies do they keep e2 nuked JFL. Your bones will mature faster when you still have the e2 variable in game. Compound - RunX2 upregulation - local aromatase production - natural test converts into e2 locally - accelerated bone maturation. Nigger what’s so fucking hard to understand if you have 0 test in your body it can’t convert locally into e2 so you don’t get a accelerated BA. What’s so fucking hard to understand? In the end you only end up with a positive.
 
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Dude I’m not even gonna keep arguing with your retarded studies. In neither of those studies do they keep e2 nuked JFL. Your bones will mature faster when you still have the e2 variable in game. Compound - RunX2 upregulation - local aromatase production - natural test converts into e2 locally - accelerated bone maturation. Nigger what’s so fucking hard to understand if you have 0 test in your body it can’t convert locally into e2 so you don’t get a accelerated BA. What’s so fucking hard to understand? In the end you only end up with a positive.
You are basing your whole argument on a theoretical situation that cannot really exist. No human can have true 0 test and 0 E2, even with letrozole or other compounds. You cant just choose those stats in real life.

But even if we magically assume you have 0 test and 0 E2, why would you then use compounds that still activate the androgen receptor? AAS are still AR agonists, meaning you are not removing androgen signaling completely that still can still lead to an increase of runx2 gene.

And im not going to sit here anymore and explain you how equations actually work in biology.

Your whole idea only works under a perfect hypothetical condition that cannot actually be achieved or measured in practice.
So my last question is, how would you actually achieve and prove this in a real human?:feelscry:
 
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5 pages of arguments
 
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You are basing your whole argument on a theoretical situation that cannot really exist. No human can have true 0 test and 0 E2, even with letrozole or other compounds. You cant just choose those stats in real life.
Dude what tf are you talking about, actually retarded. Every info you give is straight out of OpenAI:feelswhy: (we can see this with the studies you sent JFL, Fruitflies :feelsuhh:). You can't truly have 0 e2 and T, atleast we agree on something. The goal is to have as little e2 as possible, to achieve this you need as little test as possible, are you gen slow?

But even if we magically assume you have 0 test and 0 E2, why would you then use compounds that still activate the androgen receptor?
Bcs the Androgen receptor itself is net positive when the variable e2 is left out, which makes retards like you with your pseude-intelligence believe its a net negative JFL.
AAS are still AR agonists, meaning you are not removing androgen signaling completely that still can still lead to an increase of runx2 gene.
Upregulation of the RunX2 gene isn't bad really, it leads cells to a hypertrophic state (without the e2 variable). Dude I don't think you understand how RunX2 is a not net negative aslong as we have very little/close to 0 test so that it can't convert into e2 locally. BECOUSE WE WANT CELLS TO HYPERTROPHY AND NOT DIE IN THE RESTING ZONE. I can link a thread by my friend @Kojo which explains this more in depth.
And im not going to sit here anymore and explain you how equations actually work in biology.
This you: :ALOOO:
Your whole idea only works under a perfect hypothetical condition that cannot actually be achieved or measured in practice.
So my last question is, how would you actually achieve and prove this in a real human?:feelscry:
Already prooven, if we look at men with a gain of fucntion mutation in Estrogen receptors or aromatese in general, they grow up into their 30s and end up like slenderman, the only diffrence is how we get this mutation. They get it gentically which is not optimal (They have tons of issues such as osteo, neurotoxicity and more and more and more) and we get it through pharma. We would mimic the outcome of such a mutation until we achieve our desired height.
 
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Dude what tf are you talking about, actually retarded. Every info you give is straight out of OpenAI:feelswhy: (we can see this with the studies you sent JFL, Fruitflies :feelsuhh:). You can't truly have 0 e2 and T, atleast we agree on something. The goal is to have as little e2 as possible, to achieve this you need as little test as possible, are you gen slow?


Bcs the Androgen receptor itself is net positive when the variable e2 is left out, which makes retards like you with your pseude-intelligence believe its a net negative JFL.

Upregulation of the RunX2 gene isn't bad really, it leads cells to a hypertrophic state (without the e2 variable). Dude I don't think you understand how RunX2 is a not net negative aslong as we have very little/close to 0 test so that it can't convert into e2 locally. BECOUSE WE WANT CELLS TO HYPERTROPHY AND NOT DIE IN THE RESTING ZONE. I can link a thread by my friend @Kojo which explains this more in depth.

This you: :ALOOO:

Already prooven, if we look at men with a gain of fucntion mutation in Estrogen receptors or aromatese in general, they grow up into their 30s and end up like slenderman, the only diffrence is how we get this mutation. They get it gentically which is not optimal (They have tons of issues such as osteo, neurotoxicity and more and more and more) and we get it through pharma. We would mimic the outcome of such a mutation until we achieve our desired height.
Those cases dont prove that pharmacologically lowering E2 with an AI + using AAS recreates the same effect. Aromatase mutations is a genetic condition affecting the entire body from development onward, with different hormonal adaptations.
You cant assume the same outcome from a temp height stack in a normal endocrine system.

And btw you were the one using AI the whole time. Even your only study was AI linked, but ig its ok for paul to use AI and accuse others of using it 😂
 
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Those cases dont prove that pharmacologically lowering E2 with an AI + using AAS recreates the same effect.
I never said it did faggot. Its bioligically plausible and for some people its worth a try rather then LDARing

Aromatase mutations is a genetic condition affecting the entire body from development onward, with different hormonal adaptations.
You cant assume the same outcome from a temp height stack in a normal endocrine system.
Nigga why can't we assume a similar outcome when we know the basis laid on why these people grow so much?
And btw you were the one using AI the whole time. Even your only study was AI linked, but ig its ok for paul to use AI and accuse others of using it 😂
Nigha all of your studies were AI linked JFL. Im not against the use of AI, im against when its used by faggots like you (said its a study on RunX2 and linked me a study on fruit flies :ROFLMAO:)

I completely destroyed all your flawed arguments where you just asked ChatGPT what you should reply every time JFL.
 
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I never said it did faggot. Its bioligically plausible and for some people its worth a try rather then LDARing
Ahh yes this is what I wanted to hear. Sure give it a try, come back to me and tell me how it went, lmk if your gp gets stronger than steel :lul:

YOUR only Source was AI Linked, you destroyed non of my arguements, you kept repeating the same story that I understood nothing and still asked for more proof.
Your proof is Humans with a genetic aromatase defect that you are trying to replicate without understanding the mechanism at all.

gl on your cope journey
 
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Ahh yes this is what I wanted to hear. Sure give it a try, come back to me and tell me how it went, lmk if your gp gets stronger than steel :lul:

YOUR only Source was AI Linked, you destroyed non of my arguements, you kept repeating the same story that I understood nothing and still asked for more proof.
Your proof is Humans with a genetic aromatase defect that you are trying to replicate without understanding the mechanism at all.

gl on your cope journey
*decides to ignore my entire rest of the reply* KYS greycel faggot
 
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